Age-dependent Upregulation of Selenbp1 in 5XFAD Mice
- 1Department of Biological Sciences, Konkuk University, Seoul 05029 Daejeon 34134 Korea
- 2Graduate School of New Drug Discovery and Development, Chungnam National University Daejeon 34134 Korea
Abstract
Selenium-binding protein 1 (SELENBP1), previously implicated in several neurological and psychiatric disorders, was recently reported to be altered in the brains of individuals with Alzheimer’s disease (AD). However, the cellular specificity of SELENBP1 in AD pathogenesis, including its role in amyloid-beta, remains unclear. Given the prominent role of microglia in amyloid-driven neuroinflammation and the hippocampal regional vulnerability in early AD, clarifying how SELENBP1 is regulated at both regional and cell-type–specific levels is essential. In this study, we examined age- and genotype-dependent changes in Selenbp1 expression in the hippocampus and prefrontal cortex of non-transgenic and 5XFAD mice at 1.5, 3, and 6 months of age by using western blot and immunofluorescence analyses. Western blot analyses revealed robust age-dependent increases in Selenbp1 expression in both regions, with no statistically significant genotype-dependent differences. However, immunofluorescence analyses showed that Selenbp1 levels were selectively increased in amyloid-vulnerable hippocampal subregions, including the dentate gyrus, dorsal subiculum, and retrosplenial cortex. Selenbp1 expression was expressed in microglia and was largely absent from neurons or astrocytes. These findings indicate that Selenbp1 elevation under AD-like conditions is region- and cell-type–specific, reflecting microglial responses detectable only through spatially resolved analysis. Therefore, Selenbp1 may represent a microglial molecular signature associated with early amyloid pathology.
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BibTeX
@article{sim2026agedependent,
title = {{Age-dependent Upregulation of Selenbp1 in 5XFAD Mice}},
author = {Su-Yeon Sim and Soojin Kim and Yeon-Soo Kim and Jung-Soo Han},
journal = {Experimental Neurobiology},
year = {2026},
month = oct,
doi = {10.5607/en26013},
url = {https://doi.org/10.5607/en26013},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Age-dependent Upregulation of Selenbp1 in 5XFAD Mice
AU - Su-Yeon Sim
AU - Soojin Kim
AU - Yeon-Soo Kim
AU - Jung-Soo Han
PY - 2026
DA - 2026/10/31
JO - Experimental Neurobiology
DO - 10.5607/en26013
UR - https://doi.org/10.5607/en26013
AB - Selenium-binding protein 1 (SELENBP1), previously implicated in several neurological and psychiatric disorders, was recently reported to be altered in the brains of individuals with Alzheimer’s disease (AD). However, the cellular specificity of SELENBP1 in AD pathogenesis, including its role in amyloid-beta, remains unclear. Given the prominent role of microglia in amyloid-driven neuroinflammation and the hippocampal regional vulnerability in early AD, clarifying how SELENBP1 is regulated at both regional and cell-type–specific levels is essential. In this study, we examined age- and genotype-dependent changes in Selenbp1 expression in the hippocampus and prefrontal cortex of non-transgenic and 5XFAD mice at 1.5, 3, and 6 months of age by using western blot and immunofluorescence analyses. Western blot analyses revealed robust age-dependent increases in Selenbp1 expression in both regions, with no statistically significant genotype-dependent differences. However, immunofluorescence analyses showed that Selenbp1 levels were selectively increased in amyloid-vulnerable hippocampal subregions, including the dentate gyrus, dorsal subiculum, and retrosplenial cortex. Selenbp1 expression was expressed in microglia and was largely absent from neurons or astrocytes. These findings indicate that Selenbp1 elevation under AD-like conditions is region- and cell-type–specific, reflecting microglial responses detectable only through spatially resolved analysis. Therefore, Selenbp1 may represent a microglial molecular signature associated with early amyloid pathology.
SN - 1226-2560
SN - 2093-8144
ER -